Brain communications最新文献

{"title":"Thalamus anatomy predicts cognitive performance and hippocampal atrophy in aging adults: a UK Biobank study.","authors":"Guocheng Jiang, Fa-Hsuan Lin, Hugo Cogo-Moreira, Jennifer S Rabin, J Jean Chen, Walter Swardfager, Bradley J MacIntosh","doi":"10.1093/braincomms/fcaf334","DOIUrl":"10.1093/braincomms/fcaf334","url":null,"abstract":"<p><p>The thalamus has extensive inter-connectedness with different brain regions in serving cognitive processes. In a community-dwelling aging population from the United Kingdom, this study examined the independent contribution of thalamus volume loss to cognitive performances and the longitudinal anatomical relationship between the thalamus and the interconnected hippocampus. We accessed MRI data from 4348 cognitively unimpaired older adults from the UK Biobank, of whom 653 participants had follow-up MRI. We estimated regional brain volumes using T1-weighted MRI. Linear models tested the association between the thalamus volume and a cognitive composite score derived from digit-symbol substitution and trail-making tests. We used latent change score models to test the longitudinal associations between thalamus volume at baseline and the trajectory of hippocampal atrophy, and vice versa. Baseline thalamus volume was positively associated with the cognitive composite score ( <math><mi>β</mi> <mo>=</mo> <mn>0.055</mn> <mo>±</mo> <mn>0.018</mn></math> , <i>P</i> = 0.002, <i>R</i> ² = 0.09). A larger baseline thalamus volume predicted slower hippocampal atrophy ( <math><msub><mi>γ</mi> <mrow><mi>T</mi> <mo>→</mo> <mrow><mi>dH</mi></mrow> </mrow> </msub> <mo>=</mo> <mo>-</mo> <mn>0.048</mn> <mo>±</mo> <mn>0.015</mn> <mo>,</mo> <mspace></mspace> <mi>P</mi> <mo>=</mo> <mn>0.001</mn> <mo>,</mo> <mspace></mspace> <mspace></mspace> <msup><mi>R</mi> <mn>2</mn></msup> <mo>=</mo> <mn>0.09</mn></math> ), while larger hippocampal volume at baseline predicted faster thalamic atrophy ( <math><msub><mi>γ</mi> <mrow><mi>H</mi> <mo>→</mo> <mi>d</mi> <mi>T</mi></mrow> </msub> <mo>=</mo> <mn>0.043</mn> <mo>±</mo> <mn>0.022</mn> <mo>,</mo> <mspace></mspace> <mi>P</mi> <mo>=</mo> <mn>0.048</mn> <mo>,</mo> <mspace></mspace> <msup><mi>R</mi> <mn>2</mn></msup> <mo>=</mo> <mn>0.04</mn></math> ). Sex-stratified analysis revealed that hippocampal volume significantly predicted thalamic atrophy only in women. This study revealed that thalamic volume loss was associated with impaired processing speed and executive function. Thalamus and hippocampus anatomy showed bidirectional longitudinal associations and demonstrated sex differences. These findings underscore the thalamus anatomy as an important marker of brain health in the aging population.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf334"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Local field potential signal transmission is correlated with the fractional anisotropy measured by diffusion tractography.","authors":"Maral Kasiri, Sumiko Abe, Rahil Soroushmojdehi, Estefania Hernandez-Martin, Seyyed Alireza Seyyed Mousavi, Terence D Sanger","doi":"10.1093/braincomms/fcaf336","DOIUrl":"10.1093/braincomms/fcaf336","url":null,"abstract":"<p><p>In this paper we aim to examine the correlation between diffusion tensor imaging parameters of anatomical connectivity and characteristics of signal transmission obtained from patient-specific transfer function models. Here, we focused on elucidating the correlation between structural and functional neural connectivity within a cohort of pediatric patients diagnosed with dystonia. Diffusion tractography images were obtained from 12 patients with dystonia prior to the deep brain stimulation surgery. For each patient, we processed the imaging data to estimate anatomical measures including fractional anisotropy, axial diffusivity, number of fibre tracts per unit area, and fibre tract length. After the implantation of temporary depth leads for each patient as part of their treatment plan, intracranial signals were recorded. Transfer function models of local field potential recordings and the corresponding measures of functional connectivity were computed for each patient. Linear mixed effect analysis was then employed to determine the relationship between transfer function measures and diffusion tractography parameters. Our results illustrate a positive correlation between fractional anisotropy, AD, and intrinsic neural transmission measures, representing amplification and spread of intrinsic neural oscillations, obtained from the transfer functions models. However, no significant correlation was found between the functional connectivity and number of fibre tracts or fibre lengths. Our findings suggest that white matter integrity, as measured by fractional anisotropy and AD, can potentially reflect the amplification and spread of intrinsic brain signals throughout the network. This study underscores the significant relationship between structural and functional connectivity, offering valuable insights into propagation of neural activity in the brain network and potential implications for optimizing non-invasive treatments and planning for neurological disorders.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf336"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precision neuromodulation in epilepsy: from shared targets to personalized circuits.","authors":"Sandipan Pati","doi":"10.1093/braincomms/fcaf327","DOIUrl":"10.1093/braincomms/fcaf327","url":null,"abstract":"<p><p>This scientific commentary refers to 'Thalamocortical network neuromodulation for epilepsy', by Agashe <i>et al</i>. (https://doi.org/10.1093/braincomms/fcaf270).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf327"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of age on neurofilament light chain in Friedreich ataxia: a 1-year longitudinal study.","authors":"Sara Petrillo, Alessia Mongelli, Anna Castaldo, Lidia Sarro, Samuele Azzarelli, Riccardo Ronco, Barbara Castellotti, Cinzia Gellera, Fiorella Piemonte, Caterina Mariotti","doi":"10.1093/braincomms/fcaf331","DOIUrl":"10.1093/braincomms/fcaf331","url":null,"abstract":"<p><p>Friedreich's ataxia (FRDA) is a recessive inherited ataxia caused by intronic GAA repeat expansions in <i>FXN</i> gene. The repeat length is the major determinant of age at onset, usually occurring in adolescence. Clinical manifestations include progressive gait and limb ataxia, sensory loss, cardiomyopathy, and scoliosis. Neurofilament light chain protein (NfL) has been recently studied as a potential plasma biomarker for the disease. We performed a longitudinal study in 62 patients with FRDA, including 12 children (age 12-17 years) and 50 adult patients (age 18-45). The characteristics of our patient cohort largely matched those of a population mostly recruited in therapeutical clinical trials, with a mean age of 25.1 ± 8.5 years, age at onset 13.1 ± 4.8 years, and disease duration 12 ± 7 years. We found higher NfL levels in children in comparison with adult patients. Plasma concentrations remained stable at 1-year follow-up. We observed a significantly inverse correlation between plasma NfL levels and patient ages, while no correlations were found with other clinical or genetic variables. Our study confirms the typical NfL profile in FRDA patients. Our data further support the role of NfL as early indicator of axonal damage and as potential pharmacodynamic biomarker of therapeutical response especially valuable in pediatric populations.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf331"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of leukotriene receptor antagonist use on the future risk of Parkinson's disease in older patients with asthma.","authors":"Chengsheng Ju, Boqing Chen, Anette Schrag, Camille Carroll, Thomas Foltynie, Li Wei","doi":"10.1093/braincomms/fcaf340","DOIUrl":"10.1093/braincomms/fcaf340","url":null,"abstract":"<p><p>Current treatments for Parkinson's disease focus on symptom management, with no therapies yet demonstrated to slow disease progression. Leukotriene receptor antagonists, widely used for asthma, have shown potential neuroprotective effects for Parkinson's disease in preclinical studies, but have also been associated with an elevated risk of neuropsychiatric events and sleep disorders. We assessed the effect of leukotriene receptor antagonist treatment on the risk of Parkinson's disease, neuropsychiatric events, and sleep disorders in patients with asthma aged over 50 years. We conducted a cohort study using the UK Clinical Practice Research Datalink between January 2000 and December 2020. The study emulated sequential target trials (<i>n</i> = 140) using observational data, comparing leukotriene receptor antagonist treatment to no leukotriene receptor antagonist treatment among patients aged 50-84 years with asthma. The primary outcome was the risk of incident Parkinson's disease, and the secondary outcomes were neuropsychiatric events (anxiety, depression, and psychosis), and sleep disorders. Propensity score matching was employed to minimize confounding. We used pooled logistic regression models to calculate risk ratios as observational analogues of intention-to-treat and per protocol effects. A total of 97 049 matched pairs were included in the analysis, with 573 Parkinson's disease cases observed in the leukotriene receptor antagonist group and 537 in the nonleukotriene receptor antagonist group over a median follow-up of 5.9 years and 5.7 years, respectively. No significant difference in Parkinson's disease risk was observed between the two groups in either the intention-to-treat analysis [10-year risk ratio: 1.09; 95% confidence interval (CI), 0.94-1.26] or the per protocol analysis (10-year risk ratio: 0.95; 95% CI, 0.75-1.16). However, there was a higher risk of depression (intention-to-treat effect: 10-year risk ratio: 1.12; 95% CI, 1.07-1.16; number-needed-to-harm = 93; per protocol effect: 10-year risk ratio: 1.15; 95% CI, 1.08-1.22; number-needed-to-harm = 75) and sleep disorders (intention-to-treat effect: 10-year risk ratio: 1.14; 95% CI, 1.11-1.19; number-needed-to-harm = 77; per protocol effect: 10-year risk ratio: 1.12; 95% CI, 1.06-1.19; number-needed-to-harm = 88) with leukotriene receptor antagonist treatment. No clear effect was observed for anxiety or psychosis. Leukotriene receptor antagonist treatment was not associated with an altered risk of Parkinson's disease among people aged 50-84 years with asthma but was linked to a higher incidence of neuropsychiatric events.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf340"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-dependent impairment of dopamine D1 receptor signalling in mouse striatum by <i>FMR1</i> variant P626L.","authors":"Junyi Fu, Wei Jiang, Liping Shen, Jiaming Fu, Xianlai Duan, Detian Liu, Jingyi Long, Shunhua Ye, Lingjia Tang, Yong-Hong Yi, Yue-Sheng Long","doi":"10.1093/braincomms/fcaf338","DOIUrl":"10.1093/braincomms/fcaf338","url":null,"abstract":"<p><p>Non-coding CGG repeat expansions in <i>fragile X messenger ribonucleoprotein 1</i> (<i>FMR1</i>) gene lead to fragile X-related disorders. Other than the CGG repeat expansion, several <i>FMR1</i> coding variants have recently been identified to impair the molecular functions of fragile X messenger ribonucleoprotein 1 (FMRP), implicating in FMR1-associated phenotypes. This study aims to investigate the pathogenic role of a novel <i>FMR1</i> missense variant from a parkinsonism patient without the typical CGG repeat expansion. Pathogenicity of the FMRP-P626L mutant was predicted using <i>in silico</i> analysis and structural prediction. A mouse model of FMRP-P608L mutation matched with the human FMRP-P626L was established. The effects on dopamine pathway in FMRP-P608L mice were investigated using behavioural test, immunohistochemistry, ELISA, quantitative PCR (qPCR), western blotting, co-immunoprecipitation and pharmacological intervention. We identified a missense variant (c.1877 C>T, p.P626L) in coding region of <i>FMR1</i> gene from a patient diagnosed with progressive rigidity and bradykinesia, which was predicted to be a damaging mutation. The corresponding mutation (P608L) mice at 6 months old exhibited impaired motor behaviours and decreased in striatal dopamine level in an age-dependent fashion. The mutant reduced FMRP binding to G protein-coupled receptor kinase 2 (GRK2), which resulted in abnormal localization of GRK2 and impairment of dopamine D1 receptor (D1R) pathways. Administration of D1R agonist rescued the motor disabilities observed in the mutation mice. This is the first report linking a point mutation in <i>FMR1</i> to parkinsonism, demonstrating that the FMRP-P608L mutation impairs the D1R pathway by reducing its binding to GRK2. Our findings enhance the understanding of pathogenic mechanisms underlying selective functional impairment by mutations.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf338"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiregional blood-brain barrier phenotyping identifies the prefrontal cortex as the most vulnerable region to ageing in mice.","authors":"Isabel Bravo-Ferrer, Katrine Gaasdal-Bech, Chiara Colvin, Hollie J Vaughan, Jonathan Moss, Anna Williams, Blanca Díaz Castro","doi":"10.1093/braincomms/fcaf332","DOIUrl":"10.1093/braincomms/fcaf332","url":null,"abstract":"<p><p>Age-associated vascular alterations make the brain more vulnerable to neuropathologies. Research in humans and rodents has demonstrated structural, molecular, and functional alterations of the aged brain vasculature that suggest blood-brain barrier dysfunction. However, these studies focused on particular features of the blood-brain barrier and specific brain regions. Thus, it remains unclear if and which blood-brain barrier age-associated phenotypes are conserved across brain areas. Moreover, there is very limited information about how blood-brain barrier dysfunction and cell-specific phenotypes relate to each other. In this manuscript, we use immunofluorescence, transmission electron microscopy, and permeability assays to assess how age-associated blood-brain barrier molecular, structural, and functional phenotypes correlate between the blood-brain barrier cell types at three brain regions (prefrontal cortex, hippocampus, and corpus callosum) during mouse early ageing. We discovered that at 18-20 months of age, changes to the mouse blood-brain barrier are subtle. The prefrontal cortex blood-brain barrier is the most affected by age, with alterations in brain endothelial cell protein expression, blood-brain barrier permeability, basement membrane thickness, and astrocyte endfoot size when compared with young mice. Here, we deliver a detailed multicellular characterization of region-dependent blood-brain barrier changes at early stages of ageing. Our data paves the way for future studies to investigate how region-specific blood-brain barrier dysfunction may contribute to disease-associated regional vulnerability.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf332"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced beta bursting underpins loss of corticomuscular coherence in amyotrophic lateral sclerosis.","authors":"Katie Yoganathan, Michael Trubshaw, Oliver Kohl, Chetan Gohil, Irene Echeverria-Altuna, Thanuja Dharmadasa, Alicia Northall, Nahid Zokaei, David Lester, Gayle Garcia, Alexis Collins, Benazir Amein, Anna C Nobre, Kevin Talbot, Alexander G Thompson, Mark Woolrich, Martin R Turner","doi":"10.1093/braincomms/fcaf339","DOIUrl":"https://doi.org/10.1093/braincomms/fcaf339","url":null,"abstract":"<p><p>Biomarkers of disease activity that holistically capture motor system dysfunction are needed to accelerate drug discovery in amyotrophic lateral sclerosis. Magnetoencephalography is a sensitive, non-invasive measure of cortical neurophysiology. Corticomuscular coherence reflects the functional coupling of cortical oscillations with downstream muscle activity recorded by electromyography. Cortical beta frequency bursting is known to represent a core feature of the neurophysiology underpinning movement. This study aimed to characterize disruption of beta frequency activity in both cortex and muscle to refine the understanding of corticomuscular coherence loss in amyotrophic lateral sclerosis. The study analysed 42 people living with amyotrophic lateral sclerosis and 33 healthy age-matched controls. Participants undertook an isometric hand gripping task during magnetoencephalography. Muscle contraction was measured using bipolar surface electromyography recordings at both forearms. All participants performed 120 trials of the gripper task bilaterally, and 60 trials unilaterally on each side. For each trial type, the mean corticomuscular coherence over trials was calculated for each participant and the groups were compared via cluster-based permutations tests. Beta burst metrics were calculated for the motor cortex (magnetoencephalography) and flexor forearm muscles (surface electromyography) including burst fractional occupancy, burst duration and amplitude. During muscular contraction, beta frequency corticomuscular coherence from the motor cortices contralateral to the gripper task was markedly reduced in amyotrophic lateral sclerosis patients, despite no significant difference in grip strength compared with controls. Source localization analysis showed globally reduced corticomuscular coherence in amyotrophic lateral sclerosis with significant differences in the motor regions contralateral to the engaged hand. There were no significant beta frequency activity changes in the engaged-hand electromyography signal in amyotrophic lateral sclerosis compared with controls. In contrast, analysis of the cortical motor regions revealed reduced rate of beta bursting and higher amplitude during the contraction phase of the task in amyotrophic lateral sclerosis. The corticomuscular coherence disruption in amyotrophic lateral sclerosis appears driven more by cerebral pathology than by muscle denervation. Equal grip strength during the task implies compensatory pathways in disease that are not captured by corticomuscular coherence. Interneuronal dysfunction may underlie the disruption to motor cortex beta bursting. Motor cortical beta frequency metrics have potential as secondary outcome measures in therapeutic trials and need exploration as prodromal markers in asymptomatic individuals genetically predisposed to amyotrophic lateral sclerosis.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf339"},"PeriodicalIF":4.5,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12501500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145254020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the distribution of neurotransmitters to resting-state functional connectivity in Parkinson's disease.","authors":"Weihua Li, Nicholas P Lao-Kaim, Runtian Li, Antonio Martín-Bastida, Andreas-Antonios Roussakis, Graham E Searle, Natalie Valle-Guzman, Viswas Dayal, Dilan Athauda, Zinovia Kefalopoulou, Philipp Mahlknecht, Alistair Church, Kathryn J Peall, Håkan Widner, Gesine Paul, Tom Foltynie, Roger A Barker, Paola Piccini","doi":"10.1093/braincomms/fcaf308","DOIUrl":"10.1093/braincomms/fcaf308","url":null,"abstract":"<p><p>Dopamine and serotonin are two major monoamine neurotransmitters associated with Parkinson's disease (PD), but their spatial distribution and relationship to underlying functional brain architecture are not fully understood. We assessed 30 patients with PD at baseline using structural MRI, resting-state functional MRI (rs-fMRI), ¹¹C-PE2I and ¹¹C-DASB PET, along with comprehensive clinical evaluations of motor and non-motor symptoms. Of these, 15 patients with PD who completed the same assessments after 19 months were included in the longitudinal analysis. rs-fMRI was used to assess functional connectivity, while ¹¹C-PE2I and ¹¹C-DASB PET were used to evaluate interregional homogeneity of dopamine and serotonin levels, referred to as PET covariance. Functional connectivity and PET covariance were estimated using a region-of-interest (ROI)-based approach with 138 ROIs from the Automated Anatomical Labelling 3 atlas, excluding cerebellar regions. These ROIs were further grouped into eight networks: visual, sensorimotor, attention, limbic, frontoparietal, default mode, subcortical and brainstem. At baseline, linear regression revealed that functional connectivity was positively associated with both ¹¹C-PE2I PET covariance (<i>β</i>-values ranging from 0.575 to 0.790, <i>P</i> < 0.001) and ¹¹C-DASB PET covariance (<i>β</i>-values ranging from 0.356 to 0.773, <i>P</i> < 0.001) across all networks. Longitudinally, we found positive correlations between baseline functional connectivity and both ¹¹C-PE2I PET change covariance and ¹¹C-DASB PET change covariance (<i>β</i>-values ranging from 0.166 to 0.576 and 0.312 to 0.671, respectively, <i>P</i> < 0.001) across all networks. These correlations remained significant after controlling for the Euclidean distance between ROIs, indicating that the association is independent of spatial proximity. For both tracers, absolute PET uptake across seed ROIs was positively associated with correspondent regression-derived functional connectivity-PET <i>β</i>-weights, which represent the relationship between PET uptake in target ROIs and their functional connectivity to the seed. This association between target functional connectivity and PET uptake was correlated with PD motor and non-motor severity across different brain regions in a manner that was dependent on the neurotransmitter system evaluated. Our findings suggest that in patients with PD, dopamine and serotonin levels covary among brain regions that are highly functionally connected. This implies that the spatial distribution of these neurotransmitters follows the organizational principles of the brain's functional connectomes, which are associated with features of the disease.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf308"},"PeriodicalIF":4.5,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12418387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lance-Adams syndrome or chronic post-hypoxic myoclonus in adults: a systematic literature review.","authors":"Geoffroy Vellieux, Emmanuelle Apartis, Vincent Navarro","doi":"10.1093/braincomms/fcaf329","DOIUrl":"10.1093/braincomms/fcaf329","url":null,"abstract":"<p><p>Lance-Adams syndrome, or chronic post-hypoxic myoclonus, is a disabling chronic myoclonic disorder occurring in survivors of brain hypoxic events. Using a systematic methodology for literature search and data acquisition, we extensively reviewed all published cases of Lance-Adams syndrome since the first original patients were described by JW Lance and RD Adams in 1963. We analysed the available data of 272 patients extracted from the 153 included studies to summarize the natural history of Lance-Adams syndrome, outline the full spectrum of this disorder and deepen our understanding of its underlying mechanisms. Two-thirds of patients suffered from a respiratory hypoxic leading event. The main causes of anoxia were peri-surgery and anaesthetic accidents, asthma attacks/bronchospasm, cardiac disorders and intoxications/drug overdoses. Many patients exhibited a 'pure' Lance-Adams syndrome, characterized by multi-focal action-induced myoclonic jerks predominant to distal limbs. Morphologic brain imaging did not show any specific abnormalities. Neurophysiological evaluations, including EEG recordings, polymyography of myoclonus and jerk-locked back averaging of myoclonus, revealed features of cortical myoclonus in the majority of patients. Both EEG, showing epileptiform discharges on the frontal and central median regions, and brain metabolism imaging, showing hypometabolism on the pericentral regions, indicated that myoclonus in Lance-Adams syndrome originates within the motor cortex. Some anti-seizure medications have shown some effectiveness and certain neuromodulation techniques have promising effects.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf329"},"PeriodicalIF":4.5,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}